Greendale G A, Barrett-Connor E, Edelstein S, Ingles S, Haile R
Division of General Internal Medicine, UCLA School of Medicine.
J Am Geriatr Soc. 1994 Oct;42(10):1050-5. doi: 10.1111/j.1532-5415.1994.tb06208.x.
It has been proposed that high dietary sodium intake, resulting in a sodium-mediated increase in renal calcium excretion, is a risk factor for osteoporosis. To evaluate the relationship between dietary sodium intake and bone mineral density (BMD), a prospective study of the Rancho Bernardo cohort was performed.
A 24-hour diet recall was done for the period 1973 through 1975; follow-up bone mineral density of the ultradistal radius, midradius, total hip, and spine was measured between 1988 and 1991. Covariates were ascertained by self-report and examination at baseline. Multivariable analysis of the sodium-BMD association was performed using gender and menopause-specific linear regressions.
All subjects were white. At the bone evaluation, there were 258 women (average age 73.3 years) and 169 men (average age 72.4 years). In both men and women, higher levels of sodium intake were strongly associated with higher levels of calcium intake and total calories. Body mass index increased with sodium quartile in women, while a modest negative association was seen in men. In women, after age adjustment, positive associations between dietary sodium and bone density were found at the ultradistal radius (beta = 0.01, P = 0.03) and the total hip (beta = 0.019, P = 0.02). BMD increased by 0.01 to 0.02 g/cm2 per gram increase in sodium ingested. After adjustment for estrogen use, body mass, dietary calcium, alcohol, and total calories, these effects were no longer significant. Similar patterns were seen in pre- and postmenopausal women. In men, age and multivariate-adjusted BMD increased with higher sodium intake at the ultradistal radius only (beta = 0.013, P = 0.05). Stratification by gender-specific median calcium level did not significantly effect the results.
After control for confounders, a small, statistically significant protective effect of sodium was found at the ultradistal radius in men only. At other sites in women and men, no effect of sodium on BMD was apparent in the multivariable models. These results do not support a detrimental effect of dietary sodium on bone mineral density. Rather, the findings suggest that sodium intake, in the range measured, is not a major osteoporosis risk factor.
有人提出,高膳食钠摄入量会导致钠介导的肾钙排泄增加,是骨质疏松症的一个危险因素。为评估膳食钠摄入量与骨矿物质密度(BMD)之间的关系,对兰乔贝纳多队列进行了一项前瞻性研究。
对1973年至1975年期间进行了24小时饮食回顾;在1988年至1991年期间测量了超远端桡骨、桡骨中部、全髋和脊柱的随访骨矿物质密度。协变量通过基线时的自我报告和检查确定。使用性别和绝经特异性线性回归对钠与BMD关联进行多变量分析。
所有受试者均为白人。在骨评估时,有258名女性(平均年龄73.3岁)和169名男性(平均年龄72.4岁)。在男性和女性中,较高的钠摄入量都与较高的钙摄入量和总热量密切相关。女性的体重指数随钠四分位数增加,而男性中则观察到适度的负相关。在女性中,年龄调整后,在超远端桡骨(β = 0.01,P = 0.03)和全髋(β = 0.019,P = 0.02)发现膳食钠与骨密度呈正相关。摄入的钠每增加1克/厘米²,骨密度增加0.01至0.02克/厘米²。在调整了雌激素使用、体重、膳食钙、酒精和总热量后这些影响不再显著。绝经前和绝经后女性中观察到类似模式。在男性中,仅在超远端桡骨处,年龄和多变量调整后的骨密度随钠摄入量增加而增加(β = 0.013,P = 0.05)。按性别特异性钙中位数水平分层对结果无显著影响。
在控制混杂因素后,仅在男性的超远端桡骨处发现钠有微小的、具有统计学意义的保护作用。在多变量模型中,在男性和女性身体的其他部位,钠对BMD没有明显影响。这些结果不支持膳食钠对骨矿物质密度有有害影响。相反,研究结果表明在所测量范围内钠摄入不是主要的骨质疏松症危险因素。